CC10 with primary expression in the uterus and non-ciliated bronchiolar cells, has an anti-inflammatory effect on the urogenital and respiratory tracts.17,18 Deficiency of CC10 aggravates pulmonary allergic inflammation through augmentation of the TH2 response, and reconstitution of CC10 in CC10-deficient mice is able to reverse the altered phenotypes.19 These results suggested that CC10 played an important role in the development of asthma. This evidence concerns the gene SCGB1A1 and asthma.